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64 Cards in this Set

  • Front
  • Back
What is margination of leukocytes
Accumulation of leukocytes along the endothelial surface.
What mediates margination?
Mechanical and chemical mediators
What are the chemical mediators that mediate leukocyte margination?
C5a, leukotriene B4 and bacterial products
Rolling, adhesion and transmigration of leukocytes is mediated by what?
Binding of complementary adhesion molecules on leukocytes and endothelial surfaces
What are the adhesion molecules involved in leukocyte Rolling, adhesion and transmigration?
Selectins, integrins, immunoglobulins, mucin like glycoproteins.
What is the role of E- selectin and P-selectin in leukocyte rolling?
E-selcetin and P-selection are present on endothelial surface. They bind to sialyl-lewis X on leukocytes
What are the levels of selectins in the normal endothelium? During inflammation?
They are present in very low levels. During inflammation they increase in number after stimulation by specific mediator (histamine, thrombin)
Where is P-selectin stored?
Weibel palade bodies
What occurs to the distribution of P-selectin upon the activation of histamine and thrombin?
P-selectin is redistributed to the cell surface
What increases the expression of endothelial adhesion molecules ICAM-1 and VCAM-1 ?
Cytokines TNF and IL-1
What activates leukocytes to increase binding affinity of integrins?
C5a and LTB4
What do integrins bind to in the endothelial surface?
ICAM-1 and VCAM-1
What mediates the transmigration of leukocytes ?
Interaction of platelet endothelial cell adhesion molecule 1 (PECAM –1) Neutrophils release type IV collagen that degrades the basement membrane
What is chemotaxis?
The attraction of cells toward a chemical mediator that is released in the areas of inflammation
What are the important exogenous chemotactic factors Neutrophils?
Bacterial products, such as N-formyl methionine
What are the important exogenous chemotactic factors for Neutrophils?
Leukotrine B4 (LT-B4), complement system products C5a. alpha chemokines (IL-8)
What is phagocytosis?
Engulfment of particulate material bu phagocytic cells
What are the most imp. Phagocytic cells?
Neutrophils and macrophages
What are the 3 steps of phagocytosis?
Recognition and attachment. Engulfment. Killing and degradation of the ingested material
What is opsonization?
It facilitates phagocytosis, coating of particulate matter by substances referred to as opsonins
What are the 3 important opsonins?
IgG, C3b and collectins
What triggers the engulfment by phagocytes?
Binding of opsonised particle to phagocytic receptor
After binding of opsonized particle to phagocytic receptor what occurs next?
Neutrophils send out cytoplasmuc processes that surround bacteria
What is a phagolysosome?
Phagosome fuses with lysosome to form phagolysosome
What is degranulation?
Release of lysosomal contents
What is the final step in phagocytosis of microbes?
Killing and degradation
What is the most efficient bactericidal system in Neutrophils?
Oxygen dependent killing
What is the first step that occurs in oxygen dependent killing after phagocytosis has occurred
NADPH oxidase converts molecular oxygen in superoxide free radical in the presence of NADPH. Energy given off in this reaction is called respiratory burst
What mediates the less effective oxygen independent killing by Neutrophils
Substances in leukocyte granules; such as lysozyme, lactoferrin, major basic proteins, bacterial permeability increasing protein, defensins
What us responsible for the degradation of dead organisms?
Lysosomal acid hydrolases
What is a neutrophil?
Polymorphonuclear leuokocytes – key cell in acute inflammation
What receptors are present in a neutrophil,
IgG and C3b
What are the contents of a primary neutrophil granule?
Myeloperoxidase, phospholipase A2, lysozyme, acid hydrolases, elastases, defensins, bacterial permeability increasing protein.
What are the contents of secondary granules?
Phospholipase A2, lysozyme, leukocyte alkaline phosphatase, collagenase, lactoferrin, vitamin B12 binding proteins.
What is the main inflammatory cell in acute inflammation?
Neutrophils come to the site of injury within the first 24 h
What cells arrive at the site of injurt 2-3 days after injury occurs?
Monocytes-macriphages lymphocytes
What is chronic granulomatous disease of childhood?
X –linked Recessive disease. Characterized by absence of NADPH oxidase activity. Marked by phagocytic cell that ingest but not kill certain microorgs.
What are some of the characteristics of myeloperoxidase deficiency?
Autosomal recessive, infections with candida, usually little clinical consequence
What is chediak-Higashi syndrome?
AR disease, characterized by: neutropenia, albinism, cranial and peripheral neuropathy and a tendency to develop repeated infections. Presence of ab. leukocytes
What is defective in leukocyte adhesion deficiency type 1?
Defective synthesis of integrins LAF-1 and MAC –1. recurrent bacterial infections
What is defective in leukocyte adhesion deficiency type 2?
Absence of sialyl lewis X on Neutrophils. Recurrent bacterial infections
What steps are involved in the exit of neutrophils from the blood into tissues?
There are three steps: (1) In the vessel lumen: margination, rolling, and firm adhesion; (2) transmigration across the endothelium; and (3) migration in interstitial tissue toward a chemotactic stimulus
What adhesion molecules are relevant for emigration of inflammatory cells?
1) Selectins: E-selectin and P-selectin on endothelium and L-selectin on neutrophils; P- and E-selectins bind to sialyl Lewis X on the neutrophils, and L-selectin to mucin-like molecules on endothelium; (2) Immunoglobulin family molecules: ICAM-1 and VCAM-1 on endothelium bind to integrins (eg, LFA-1, Mac-1, and VLA-4) on leukocytes.
At what stages do they function?
Selectins are involved in rolling. Integrins are involved in firm adhesion. PECAM-1, another adhesion molecule expressed on both leukocytes and endothelial cells, is involved in transmigration.
What mechanisms do neutrophils use to kill microbes?
Two mechanisms are used: (1) oxygen-dependent and (2) oxygen-independent. Oxygen-dependent mechanisms are the most important. They involve generation of superoxide O2- via the NADPH system. This gives rise eventually to H2O2 and OH-. Also generated are myeloperoxidase-dependent HOCl- radicals. Oxygen-independent mechanisms include lysozyme, lactoferrin, and defensins
Do you know of any defects in neutrophil killing mechanisms?
Three important defects are (1) defects in adhesion due to genetic deficiency of B2 integrins (LAD-1); (2) defects in chemotaxis or phagocytosis from an inherited impairment in assembly of microtubules (eg, Chediak-Higashi syndrome); (3) defects in microbicidal activity due to a genetic deficiency of the NADPH oxidase system (called chronic granulomatous disease) or genetic deficiency of myeloperoxidase.
What is acute salpingitis?
Acute inflammation of fallopian tubes
What are some examples of harmful effects of repair?
Formation of scars, disfigurement, intestinal obstruction.
What are some of the characteristics of acute inflammation?
Early response to injury, infection chemical agents. Rapid onset, short duration, exudation, accumulation of neutrophils
What are some of the characteristics that help distinguish from acute and chronic inflammation?
Longer duration, influx of lymphocytes and macrophages
The escape of fluid, proteins and blood cells from the vascular system into the interstitial tissue or body cavities.
An inflammatory extravascular fluid with a high protein concentration. Implies sig. Alteration in permeability of small blood vessels inan area of injury
Extravascular fluid with a low protein content few or no cells. Results due imbalence in hydrostatic pressure.
Excess amount of fluis in interstitial spaces or body cavities. Can be exudates or transudate
Purulent exudates is inflammatory rich in neutrophil and debris of dead cells
What is the purpose of inflammation?
To get Neutrophils to the site of injury. To celar the invading organism and begin the process of healing
What are the 5 cardinal signs of acute inflammation?
Calor, rubor, tumor, dolor, functio laesa
What is the mechanism of calor in inflammation?
Heat- histamine dependent vasodilation
What is the mechanism of rubor in inflammation?
Redness- histamine dependent vasodialtion
What is the mechanism of tumor in inflammation?
Swelling- histamine dependent increase in vascular permeability
What is the mechanism of doloe in inflammation?
Pain- due to prostaglandin E2 and bradykinin
What causes the vasodilation in inflammation?
Mast cells release histamine which acts on vascular smooth muscle cells.
What causes the increase in permeability of venules in inflammation?
Histamine contracts endothelial cells, causing movemnt of fluid into interstitial tissue.
What causes stasis in inflammation?
The outflow of fluid form the blood vessels‡ increase viscosity. Rouleau formation, alteration in lamina flow, neutrophil margination